Kuppers, R., Sonoki, T., Satterwhite, E., Gesk, S., Harder, L., Oscier, D. G., Tucker, P.W., Dyer, M. J.S. and Siebert, R., 2002. Lack of somatic hypermutation of IG V<sub>H</sub> genes in lymphoid malignancies with t(2;14)(p13;q32) translocation involving the BCL11A gene. Leukemia, 16 (5), pp. 937-939.
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The t(2;14)(p13;q32.3) involving the BCL11A and IGH genes is a rare but recurrent chromosomal aberration in B-cell malignancies. Hitherto, juxtaposition of BCL11A and IGH has only been described in B-cell chronic lymphocytic leukemia (B-CLL) and immunocytoma. As subgroups of B-CLL can be distinguished by the pattern of somatic mutation of immunoglobulin variable (V) genes we investigated four lymphomas with IGH/BCL11A involvement for IGH hypermutation. Clonal V[SUPH] gene rearrangements were amplified; in all four cases, sequencing of the amplificates revealed the rearranged V[SUPH] genes to lack somatic mutations. These results suggest that t(2;14)(p13;q32.3) is associated with a subset of B-CLL/immunocytoma characterized by non-mutated IG genes deriving from pre-germinal center B cells. As the translocations in both informative cases are targeted to the switch regions of the IGG2 gene, which is mainly used in T cell-independent immune responses, these translocations presumably occurred in activated B cells in the course of T cell-independent immune responses outside the germinal center.
|Subjects:||Technology > Medicine and Health|
|Group:||School of Health and Social Care > Centre for Postgraduate Medical Research and Education|
|Deposited By:||INVALID USER|
|Deposited On:||19 Oct 2008 20:23|
|Last Modified:||07 Mar 2013 14:51|
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